Do PPAR Ligands Suppress the Growth of Cholangiocarcinoma or the Cholangiohepatitis Induced by the Tumor?
Figure 1
Inhibitory effects of PPARγ ligand on the
development of cholangiocarcinoma. PPARγ ligand directly suppresses tumor progression through
p53 and Smad pathways (red arrow) and also stimulates adipocyte and
hepatobiliary cells (gray arrow). Secretion of adipokines (TNF-α, adiponectin, and leptin) and production of
lipid-related proteins (FABP and LPL) are regulated by PPARγ ligand. Up- and downregulation of various gene signals
from adipocytes (yellow line) and hepatobiliary cells (broken line) promoted
suppression of tumor growth. As a result, PPARγ
indirectly suppressed tumor growth of cholangiocarcinoma through adipocytes and
hepatobiliary cells. Currently, evidence of suppressive signals from
hepatobiliary cells to cholangiocarcinoma is unavailable (broken line). FABP:
fatty acid binding protein, LPL: lipoprotein lipase, TNF-α: tumor necrosis factor-α.